| 2013 |
GNA13 knockdown in highly invasive PC3 prostate cancer cells inhibits invasion, migration, and Rho activation, establishing GNA13 as a required mediator of RhoA activity downstream of GPCRs in these cells. miR-182 and miR-141/200a directly target the 3'-UTR of GNA13, post-transcriptionally suppressing its expression and reducing invasion; restoration of GNA13 blocks this effect. |
siRNA knockdown, 3'-UTR luciferase reporter assay, Boyden chamber invasion assay, miRNA inhibitors, ectopic miRNA expression |
The Journal of biological chemistry |
Medium |
23329838
|
| 2014 |
GNA13 is a direct target of miR-29c; miR-29c suppresses GNA13 expression and consequently inhibits EMT in colorectal cancer cells through the ERK/GSK3β/β-catenin pathway. |
qRT-PCR, in vitro invasion/migration assays, in vivo metastasis assay, miRNA target validation, pathway analysis |
Annals of oncology |
Medium |
25193986
|
| 2015 |
GNA13 expression in breast cancer cells is post-transcriptionally controlled by miR-31, which directly targets the GNA13 3'-UTR. Overexpression of GNA13 in MCF-10a cells induces invasion; knockdown in MDA-MB-231 cells inhibits invasion. Rescue of GNA13 in miR-31-expressing cells partially restores invasion. |
3'-UTR luciferase reporter assay, RT-PCR, Western blotting, Boyden chamber invasion assay, ectopic miR-31 expression, miR-31 inhibitors |
Molecular cancer |
Medium |
25889182
|
| 2015 |
Cancer-specific GNA13 mutations identified in Burkitt's lymphoma and DLBCL are inhibitory (loss-of-function) in nature. Re-expression of wild-type Gα13 in B-cell lymphoma cells bearing mutant GNA13 causes remarkable growth inhibition in vivo, but has limited impact in vitro, supporting a tumor suppressor role for the Gα13/RhoA axis in B cells. |
Multiple complementary functional approaches (in vitro and in vivo), mutant characterization, re-expression of wild-type GNA13 |
Oncogene |
Medium |
26616858
|
| 2016 |
Conditional knockout of GNA13 in germinal center B cells (AID-Cre model) leads to disordered GC architecture, altered migration, decreased filamentous actin, attenuated RhoA activity, impaired caspase-mediated apoptosis, and increased somatic hypermutation. Combined with MYC transgene, GNA13 deficiency promotes lymphomagenesis, establishing a tumor suppressor role for GNA13 in GC B cells. |
Conditional knockout mouse model (AID-Cre × Gna13 flox), in vivo GC architecture analysis, in vitro migration assay, RhoA activity assay, caspase activity assay, immunoglobulin VH somatic hypermutation analysis |
Blood |
High |
26989201
|
| 2016 |
Enhanced GNA13 signaling in MCF-10a breast cells suppresses transcription of tumor-protective Kallikrein genes (KLK5, KLK6, KLK7, KLK8, KLK10) via negative regulation of RhoA/ROCK signaling. Rhotekin pulldown confirmed that GNA13 overexpression reduces active RhoA; blocking RhoA with C3-toxin or ROCK inhibitor phenocopies GNA13-mediated KLK suppression. |
Microarray, real-time PCR, promoter luciferase assay, Rhotekin pulldown (RhoA activity assay), C3-toxin and ROCK inhibitor treatment, GNA13 knockdown in MDA-MB-157 cells |
Cellular signalling |
Medium |
27424208
|
| 2018 |
GNA13 overexpression in colorectal cancer cells activates the NF-κB/p65 signaling pathway, leading to upregulation of chemokines CXCL1, CXCL2, and CXCL4, which promote proliferation and angiogenesis. NF-κB/p65 inhibition abrogates GNA13-induced migration, invasion, and chemokine upregulation. |
GNA13 overexpression/knockdown, Western blotting, NF-κB inhibitor treatment, ELISA/chemokine measurement, cell growth and invasion assays |
Cancer medicine |
Medium |
30267476
|
| 2021 |
GNA13 undergoes palmitoylation that is essential for its plasma membrane localization and stability in GCB-DLBCL cells. Palmitoylation-dependent membrane localization is required for GNA13's tumor suppressor function. GNA13 negatively regulates BCL2 expression in a palmitoylation-dependent manner; loss of palmitoylation abrogates GNA13-mediated BCL2 suppression. |
Palmitoylation assay, subcellular fractionation, GNA13 mutant overexpression (palmitoylation-deficient), Western blotting for BCL2, cell viability assay with BCL2 inhibitor |
Cell death & disease |
Medium |
33423045
|
| 2021 |
GNA13 overexpression in glioma cells downregulates PRKACA (a PKA subunit), leading to reduced phosphorylation of RELA and decreased MGMT expression, sensitizing glioma cells to temozolomide through the GNA13/PRKACA/p-RELA and GNA13/PRKACA/MGMT signaling axes. |
GNA13 overexpression, Western blotting for PRKACA, p-RELA, MGMT, bioinformatic analysis (GSE80729, GSE43452), cell viability assay with TMZ |
American journal of translational research |
Low |
34786068
|
| 2023 |
GNA13 acts upstream of the ERK signaling pathway in glioblastoma cells; GNA13 knockdown increases ERK phosphorylation and promotes migration/invasion, while GNA13 overexpression inhibits ERK phosphorylation and suppresses metastasis. GNA13 regulates FOXO3 as a downstream effector of ERK, and the ERK inhibitor U0126 rescues the pro-metastatic phenotype induced by GNA13 knockdown. |
GNA13 knockdown/overexpression, Western blotting for p-ERK, pharmacological epistasis with U0126 (ERK inhibitor), qRT-PCR for FOXO3, migration/invasion assays |
Cellular signalling |
Medium |
37392861
|
| 2024 |
GNA13 suppresses proliferation in ER+ breast cancer cells via an ERα-dependent mechanism that regulates MYC expression at both transcript and protein levels. Loss of GNA13 upregulates MYC signaling pathways; simultaneous silencing of MYC reverses the proliferative effect caused by GNA13 loss, demonstrating epistasis between GNA13 and MYC downstream of ERα. |
GNA13 knockdown/overexpression, RNA-sequencing, MYC co-silencing (genetic epistasis), orthotopic xenograft model, soft-agar colony formation assay, Western blotting |
Breast cancer research : BCR |
Medium |
38965558
|
| 2025 |
A gain-of-function R200K missense mutation in GNA13 hyperactivates the RHOA/ROCK signaling pathway, increasing actin polymerization and myosin light chain phosphorylation, promoting melanocyte rounding and impairing cell migration/adhesion without affecting proliferation. R200K Gα13 also hyperactivates the YAP signaling pathway. The resulting defect in melanosome transfer to keratinocytes causes hypopigmentation. |
In-depth functional investigations in patient-derived cells, actin polymerization assay, myosin light chain phosphorylation Western blot, cell morphology and migration assay, YAP pathway analysis, comparison to wild-type GNA13 |
Nature communications |
Medium |
39966435
|
| 2025 |
DHHC13 (zinc finger DHHC-type palmitoyltransferase 13) catalyzes S-palmitoylation of GNA13 at Cys14 and Cys18 residues in Sertoli cells, which is required for GNA13 plasma membrane localization and its selective enrichment in Sertoli cell-derived extracellular vesicles. Palmitoylated GNA13 delivered via EVs to spermatogonial stem cells suppresses autophagy through interaction with ARHGEF12, promoting RhoA activity; inhibition of GNA13 palmitoylation reduces ARHGEF12 interaction, diminishes RhoA activity, and elevates autophagy. |
Site-directed mutagenesis of palmitoylation sites (Cys14/Cys18), palmitoylation assay, subcellular fractionation, EV isolation, Co-immunoprecipitation (GNA13–ARHGEF12 interaction), RhoA activity assay, autophagy assay |
Cell communication and signaling : CCS |
Medium |
40205436
|
| 2022 |
GNA13 knockdown in lung squamous cell carcinoma cells reduces phosphorylation of PI3K and AKT, while GNA13 overexpression increases PI3K/AKT phosphorylation, placing GNA13 upstream of the PI3K/AKT pathway in regulating LUSC cell growth and migration. |
GNA13 siRNA knockdown and overexpression, Western blotting for p-PI3K and p-AKT, MTT assay, wound healing, Transwell invasion assay, in vivo LUSC mouse model |
Tissue & cell |
Low |
35413491
|